SFEEU2025 Society for Endocrinology Clinical Update 2025 Workshop B: Disorders of growth and development (7 abstracts)
Cambridge University Hospital, Cambridge, United Kingdom
Introduction: Hypogonadotropic hypogonadism(HH) is characterized by low gonadotropin(LH and FSH) secretion, resulting in impaired gonadal function, delayed or absent puberty, and underdeveloped secondary sexual characteristics. It can be congenital or acquired, necessitating careful evaluation and tailored treatment. This case report details the clinical course and management of an 18-year-old male who presented to the adult endocrine service.
Case Presentation: An 18-year-old male was referred for delayed growth, with a height of 1.72 m, weight of 57 kg, and a mid-parental height of 176.50193.50 cm. Laboratory studies showed undetectable LH, low FSH, and very low testosterone, with normal other anterior pituitary hormones. Physical exam revealed Tanner stage-2, an unpalpable right testis in the inguinal canal, and a left testis measuring 1-2 ml. MRI showed a normal pituitary. Bone age was delayed at 14-years, compared to his chronological age of 18. After discussion with the patient and his family, the decision was made to commence puberty induction treatment with gonadotropins rather than testosterone. A previously scheduled orchidopexy was withheld, and he was started on treatment with FSH. Testicular volumes and penile size increased within the next 2-3 months, and treatment with hCG was added. Over subsequent months, testicular size continued to increase, he progressed to Tanner stage-3, his height reached 180 cm. The right testis descended into the scrotum. Treatment doses was adjusted due to increased oestradiol levels and, mild gynecomastia but they both resolved after reduction of hCG, while pubertal development continued.
Discussion: This case highlights the challenges in managing HH presenting in late adolescence. Thorough evaluation confirmed HH with a normal pituitary. Gonadotropin therapy gradually promoted testicular growth, secondary sexual development, and spontaneous testicular descent.
| 06/10/23 | 30/01/24 | 12/04/24 | 07/06/24 | 18/06/24 | 17/07/24 | |
| IGF-1 | 19.8 | 20.7 | 43.0 | |||
| LH | 1.1(L) | 1.5 | <0.2 | <0.2 | ||
| FSH | 1.9 | 2.1 | 7.5 | 1.2 | 4.2 | |
| Oestradiol | <78 | 137 | 275 | |||
| Testosterone(Male-Adult) | 1.6 | 0.9 | 3.8 | 37.5 | 17.7 | 40.7 |
| 07/03/25 | 24/04/25 | |
| LH | <0.2 | 2.8 |
| FSH | 1.4 | 6.0 |
| Oestradiol | 144 | 89 |
| Testosterone (Male-Adult) | 8.3 | 9.1 |
| ReferenceIGF-1 15.2-42.0 nmol/lLH 1.5 -9.3 U/lFSH 1.4-18.1 U/lOestradiol 0-146 pmol/lTestosterone 7.9-31.3 nmol/l | ||
Conclusion: While male puberty induction treatment traditionally included testosterone treatment, Gonadotropin therapy can increase the chances of future fertility, while still promoting testicular growth, secondary sexual development, and, as shown in our patient, spontaneous testicular descent. Early diagnosis and personalized management are key to optimizing puberty and fertility, with ongoing assessment of testicular function and semen parameters necessary for future reproductive planning.